In The Fake News Era, Are We Too Gullible? No, Says Cognitive Scientist
One of the oddest political hoaxes of recent times was Pizzagate, in which conspiracy theorists claimed that Hillary Clinton and her 2016 campaign chief ran a child sex ring from the basement of a Washington, DC, pizzeria.
To fight disinformation more effectively, he suggests, humans need to stop believing in one thing above all: our own gullibility.
Millions of believers spread the rumor on social media, abetted by Russian bots; one outraged netizen stormed the restaurant with an assault rifle and shot open what he took to be the dungeon door. (It actually led to a computer closet.) Pundits cited the imbroglio as evidence that Americans had lost the ability to tell fake news from the real thing, putting our democracy in peril.
Such fears, however, are nothing new. "For most of history, the concept of widespread credulity has been fundamental to our understanding of society," observes Hugo Mercier in Not Born Yesterday: The Science of Who We Trust and What We Believe (Princeton University Press, 2020). In the fourth century BCE, he points out, the historian Thucydides blamed Athens' defeat by Sparta on a demagogue who hoodwinked the public into supporting idiotic military strategies; Plato extended that argument to condemn democracy itself. Today, atheists and fundamentalists decry one another's gullibility, as do climate-change accepters and deniers. Leftists bemoan the masses' blind acceptance of the "dominant ideology," while conservatives accuse those who do revolt of being duped by cunning agitators.
What's changed, all sides agree, is the speed at which bamboozlement can propagate. In the digital age, it seems, a sucker is born every nanosecond.
The Case Against Credulity
Yet Mercier, a cognitive scientist at the Jean Nicod Institute in Paris, thinks we've got the problem backward. To fight disinformation more effectively, he suggests, humans need to stop believing in one thing above all: our own gullibility. "We don't credulously accept whatever we're told—even when those views are supported by the majority of the population, or by prestigious, charismatic individuals," he writes. "On the contrary, we are skilled at figuring out who to trust and what to believe, and, if anything, we're too hard rather than too easy to influence."
He bases those contentions on a growing body of research in neuropsychiatry, evolutionary psychology, and other fields. Humans, Mercier argues, are hardwired to balance openness with vigilance when assessing communicated information. To gauge a statement's accuracy, we instinctively test it from many angles, including: Does it jibe with what I already believe? Does the speaker share my interests? Has she demonstrated competence in this area? What's her reputation for trustworthiness? And, with more complex assertions: Does the argument make sense?
This process, Mercier says, enables us to learn much more from one another than do other animals, and to communicate in a far more complex way—key to our unparalleled adaptability. But it doesn't always save us from trusting liars or embracing demonstrably false beliefs. To better understand why, leapsmag spoke with the author.
How did you come to write Not Born Yesterday?
In 2010, I collaborated with the cognitive scientist Dan Sperber and some other colleagues on a paper called "Epistemic Vigilance," which laid out the argument that evolutionarily, it would make no sense for humans to be gullible. If you can be easily manipulated and influenced, you're going to be in major trouble. But as I talked to people, I kept encountering resistance. They'd tell me, "No, no, people are influenced by advertising, by political campaigns, by religious leaders." I started doing more research to see if I was wrong, and eventually I had enough to write a book.
With all the talk about "fake news" these days, the topic has gotten a lot more timely.
Yes. But on the whole, I'm skeptical that fake news matters very much. And all the energy we spend fighting it is energy not spent on other pursuits that may be better ways of improving our informational environment. The real challenge, I think, is not how to shut up people who say stupid things on the internet, but how to make it easier for people who say correct things to convince people.
"History shows that the audience's state of mind and material conditions matter more than the leader's powers of persuasion."
You start the book with an anecdote about your encounter with a con artist several years ago, who scammed you out of 20 euros. Why did you choose that anecdote?
Although I'm arguing that people aren't generally gullible, I'm not saying we're completely impervious to attempts at tricking us. It's just that we're much better than we think at resisting manipulation. And while there's a risk of trusting someone who doesn't deserve to be trusted, there's also a risk of not trusting someone who could have been trusted. You miss out on someone who could help you, or from whom you might have learned something—including figuring out who to trust.
You argue that in humans, vigilance and open-mindedness evolved hand-in-hand, leading to a set of cognitive mechanisms you call "open vigilance."
There's a common view that people start from a state of being gullible and easy to influence, and get better at rejecting information as they become smarter and more sophisticated. But that's not what really happens. It's much harder to get apes than humans to do anything they don't want to do, for example. And research suggests that over evolutionary time, the better our species became at telling what we should and shouldn't listen to, the more open to influence we became. Even small children have ways to evaluate what people tell them.
The most basic is what I call "plausibility checking": if you tell them you're 200 years old, they're going to find that highly suspicious. Kids pay attention to competence; if someone is an expert in the relevant field, they'll trust her more. They're likelier to trust someone who's nice to them. My colleagues and I have found that by age 2 ½, children can distinguish between very strong and very weak arguments. Obviously, these skills keep developing throughout your life.
But you've found that even the most forceful leaders—and their propaganda machines—have a hard time changing people's minds.
Throughout history, there's been this fear of demagogues leading whole countries into terrible decisions. In reality, these leaders are mostly good at feeling the crowd and figuring out what people want to hear. They're not really influencing [the masses]; they're surfing on pre-existing public opinion. We know from a recent study, for instance, that if you match cities in which Hitler gave campaign speeches in the late '20s through early '30s with similar cities in which he didn't give campaign speeches, there was no difference in vote share for the Nazis. Nazi propaganda managed to make Germans who were already anti-Semitic more likely to express their anti-Semitism or act on it. But Germans who were not already anti-Semitic were completely inured to the propaganda.
So why, in totalitarian regimes, do people seem so devoted to the ruler?
It's not a very complex psychology. In these regimes, the slightest show of discontent can be punished by death, or by you and your whole family being sent to a labor camp. That doesn't mean propaganda has no effect, but you can explain people's obedience without it.
What about cult leaders and religious extremists? Their followers seem willing to believe anything.
Prophets and preachers can inspire the kind of fervor that leads people to suicidal acts or doomed crusades. But history shows that the audience's state of mind and material conditions matter more than the leader's powers of persuasion. Only when people are ready for extreme actions can a charismatic figure provide the spark that lights the fire.
Once a religion becomes ubiquitous, the limits of its persuasive powers become clear. Every anthropologist knows that in societies that are nominally dominated by orthodox belief systems—whether Christian or Muslim or anything else—most people share a view of God, or the spirit, that's closer to what you find in societies that lack such religions. In the Middle Ages, for instance, you have records of priests complaining of how unruly the people are—how they spend the whole Mass chatting or gossiping, or go on pilgrimages mostly because of all the prostitutes and wine-drinking. They continue pagan practices. They resist attempts to make them pay tithes. It's very far from our image of how much people really bought the dominant religion.
"The mainstream media is extremely reliable. The scientific consensus is extremely reliable."
And what about all those wild rumors and conspiracy theories on social media? Don't those demonstrate widespread gullibility?
I think not, for two reasons. One is that most of these false beliefs tend to be held in a way that's not very deep. People may say Pizzagate is true, yet that belief doesn't really interact with the rest of their cognition or their behavior. If you really believe that children are being abused, then trying to free them is the moral and rational thing to do. But the only person who did that was the guy who took his assault weapon to the pizzeria. Most people just left one-star reviews of the restaurant.
The other reason is that most of these beliefs actually play some useful role for people. Before any ethnic massacre, for example, rumors circulate about atrocities having been committed by the targeted minority. But those beliefs aren't what's really driving the phenomenon. In the horrendous pogrom of Kishinev, Moldova, 100 years ago, you had these stories of blood libel—a child disappeared, typical stuff. And then what did the Christian inhabitants do? They raped the [Jewish] women, they pillaged the wine stores, they stole everything they could. They clearly wanted to get that stuff, and they made up something to justify it.
Where do skeptics like climate-change deniers and anti-vaxxers fit into the picture?
Most people in most countries accept that vaccination is good and that climate change is real and man-made. These ideas are deeply counter-intuitive, so the fact that scientists were able to get them across is quite fascinating. But the environment in which we live is vastly different from the one in which we evolved. There's a lot more information, which makes it harder to figure out who we can trust. The main effect is that we don't trust enough; we don't accept enough information. We also rely on shortcuts and heuristics—coarse cues of trustworthiness. There are people who abuse these cues. They may have a PhD or an MD, and they use those credentials to help them spread messages that are not true and not good. Mostly, they're affirming what people want to believe, but they may also be changing minds at the margins.
How can we improve people's ability to resist that kind of exploitation?
I wish I could tell you! That's literally my next project. Generally speaking, though, my advice is very vanilla. The mainstream media is extremely reliable. The scientific consensus is extremely reliable. If you trust those sources, you'll go wrong in a very few cases, but on the whole, they'll probably give you good results. Yet a lot of the problems that we attribute to people being stupid and irrational are not entirely their fault. If governments were less corrupt, if the pharmaceutical companies were irreproachable, these problems might not go away—but they would certainly be minimized.
Leading XPRIZE Healthspan and Beating Negativity with Dr. Peter Diamandis
A new competition by the XPRIZE Foundation is offering $101 million to researchers who discover therapies that give a boost to people aged 65-80 so their bodies perform more like when they were middle-aged.
For today’s podcast episode, I talked with Dr. Peter Diamandis, XPRIZE’s founder and executive chairman. Under Peter’s leadership, XPRIZE has launched 27 previous competitions with over $300 million in prize purses. The latest contest aims to enhance healthspan, or the period of life when older people can play with their grandkids without any restriction, disability or disease. Such breakthroughs could help prevent chronic diseases that are closely linked to aging. These illnesses are costly to manage and threaten to overwhelm the healthcare system, as the number of Americans over age 65 is rising fast.
In this competition, called XPRIZE Healthspan, multiple awards are available, depending on what’s achieved, with support from the nonprofit Hevolution Foundation and Chip Wilson, the founder of Lululemon and nonprofit SOLVE FSHD. The biggest prize, $81 million, is for improvements in cognition, muscle and immunity by 20 years. An improvement of 15 years will net $71 million, and 10 years will net $61 million.
In our conversation for this episode, Peter talks about his plans for XPRIZE Healthspan and why exponential technologies make the current era - even with all of its challenges - the most exciting time in human history. We discuss the best mental outlook that supports a person in becoming truly innovative, as well as the downsides of too much risk aversion. We talk about how to overcome the negativity bias in ourselves and in mainstream media, how Peter has shifted his own mindset to become more positive over the years, how to inspire a culture of innovation, Peter’s personal recommendations for lifestyle strategies to live longer and healthier, the innovations we can expect in various fields by 2030, the future of education and the importance of democratizing tech and innovation.
In addition to Peter’s pioneering leadership of XPRIZE, he is also the Executive Founder of Singularity University. In 2014, he was named by Fortune as one of the “World’s 50 Greatest Leaders.” As an entrepreneur, he’s started over 25 companies in the areas of health-tech, space, venture capital and education. He’s Co-founder and Vice-Chairman of two public companies, Celularity and Vaxxinity, plus being Co-founder & Chairman of Fountain Life, a fully-integrated platform delivering predictive, preventative, personalized and data-driven health. He also serves as Co-founder of BOLD Capital Partners, a venture fund with a half-billion dollars under management being invested in exponential technologies and longevity companies. Peter is a New York Times Bestselling author of four books, noted during our conversation and in the show notes of this episode. He has degrees in molecular genetics and aerospace engineering from MIT and holds an M.D. from Harvard Medical School.
Show links
- Peter Diamandis bio
- New XPRIZE Healthspan
- Peter Diamandis books
- 27 XPRIZE competitions and counting
- Life Force by Peter Diamandis and Tony Robbins
- Peter Diamandis Twitter
- Longevity Insider newsletter – AI identifies the news
- Peter Diamandis Longevity Handbook
- Hevolution funding for longevity
XPRIZE Founder Peter Diamandis speaks with Mehmoud Khan, CEO of Hevolution Foundation, at the launch of XPRIZE Healthspan.
Hevolution Foundation
From infections with no symptoms to why men are more likely to be hospitalized in the ICU and die of COVID-19, new research shows that your genes play a significant role
Early in the pandemic, genetic research focused on the virus because it was readily available. Plus, the virus contains only 30,000 bases in a dozen functional genes, so it's relatively easy and affordable to sequence. Additionally, the rapid mutation of the virus and its ability to escape antibody control fueled waves of different variants and provided a reason to follow viral genetics.
In comparison, there are many more genes of the human immune system and cellular functions that affect viral replication, with about 3.2 billion base pairs. Human studies require samples from large numbers of people, the analysis of each sample is vastly more complex, and sophisticated computer analysis often is required to make sense of the raw data. All of this takes time and large amounts of money, but important findings are beginning to emerge.
Asymptomatics
About half the people exposed to SARS-CoV-2, the virus that causes the COVID-19 disease, never develop symptoms of this disease, or their symptoms are so mild they often go unnoticed. One piece of understanding the phenomena came when researchers showed that exposure to OC43, a common coronavirus that results in symptoms of a cold, generates immune system T cells that also help protect against SARS-CoV-2.
Jill Hollenbach, an immunologist at the University of California at San Francisco, sought to identify the gene behind that immune protection. Most COVID-19 genetic studies are done with the most seriously ill patients because they are hospitalized and thus available. “But 99 percent of people who get it will never see the inside of a hospital for COVID-19,” she says. “They are home, they are not interacting with the health care system.”
Early in the pandemic, when most labs were shut down, she tapped into the National Bone Marrow Donor Program database. It contains detailed information on donor human leukocyte antigens (HLAs), key genes in the immune system that must match up between donor and recipient for successful transplants of marrow or organs. Each HLA can contain alleles, slight molecular differences in the DNA of the HLA, which can affect its function. Potential HLA combinations can number in the tens of thousands across the world, says Hollenbach, but each person has a smaller number of those possible variants.
She teamed up with the COVID-19 Citizen Science Study a smartphone-based study to track COVID-19 symptoms and outcomes, to ask persons in the bone marrow donor registry about COVID-19. The study enlisted more than 30,000 volunteers. Those volunteers already had their HLAs annotated by the registry, and 1,428 tested positive for the virus.
Analyzing five key HLAs, she found an allele in the gene HLA-B*15:01 that was significantly overrepresented in people who didn’t have any symptoms. The effect was even stronger if a person had inherited the allele from both parents; these persons were “more than eight times more likely to remain asymptomatic than persons who did not carry the genetic variant,” she says. Altogether this HLA was present in about 10 percent of the general European population but double that percentage in the asymptomatic group. Hollenbach and her colleagues were able confirm this in other different groups of patients.
What made the allele so potent against SARS-CoV-2? Part of the answer came from x-ray crystallography. A key element was the molecular shape of parts of the cold virus OC43 and SARS-CoV-2. They were virtually identical, and the allele could bind very tightly to them, present their molecular antigens to T cells, and generate an extremely potent T cell response to the viruses. And “for whatever reasons that generated a lot of memory T cells that are going to stick around for a long time,” says Hollenbach. “This T cell response is very early in infection and ramps up very quickly, even before the antibody response.”
Understanding the genetics of the immune response to SARS-CoV-2 is important because it provides clues into the conditions of T cells and antigens that support a response without any symptoms, she says. “It gives us an opportunity to think about whether this might be a vaccine design strategy.”
Dead men
A researcher at the Leibniz Institute of Virology in Hamburg Germany, Guelsah Gabriel, was drawn to a question at the other end of the COVID-19 spectrum: why men more likely to be hospitalized and die from the infection. It wasn't that men were any more likely to be exposed to the virus but more likely, how their immune system reacted to it
Several studies had noted that testosterone levels were significantly lower in men hospitalized with COVID-19. And, in general, the lower the testosterone, the worse the prognosis. A year after recovery, about 30 percent of men still had lower than normal levels of testosterone, a condition known as hypogonadism. Most of the men also had elevated levels of estradiol, a female hormone (https://pubmed.ncbi.nlm.nih.gov/34402750/).
Every cell has a sex, expressing receptors for male and female hormones on their surface. Hormones docking with these receptors affect the cells' internal function and the signals they send to other cells. The number and role of these receptors varies from tissue to tissue.
Gabriel began her search by examining whole exome sequences, the protein-coding part of the genome, for key enzymes involved in the metabolism of sex hormones. The research team quickly zeroed in on CYP19A1, an enzyme that converts testosterone to estradiol. The gene that produces this enzyme has a number of different alleles, the molecular variants that affect the enzyme's rate of metabolizing the sex hormones. One genetic variant, CYP19A1 (Thr201Met), is typically found in 6.2 percent of all people, both men and women, but remarkably, they found it in 68.7 percent of men who were hospitalized with COVID-19.
Lung surprise
Lungs are the tissue most affected in COVID-19 disease. Gabriel wondered if the virus might be affecting expression of their target gene in the lung so that it produces more of the enzyme that converts testosterone to estradiol. Studying cells in a petri dish, they saw no change in gene expression when they infected cells of lung tissue with influenza and the original SARS-CoV viruses that caused the SARS outbreak in 2002. But exposure to SARS-CoV-2, the virus responsible for COVID-19, increased gene expression up to 40-fold, Gabriel says.
Did the same thing happen in humans? Autopsy examination of patients in three different cites found that “CYP19A1 was abundantly expressed in the lungs of COVID-19 males but not those who died of other respiratory infections,” says Gabriel. This increased enzyme production led likely to higher levels of estradiol in the lungs of men, which “is highly inflammatory, damages the tissue, and can result in fibrosis or scarring that inhibits lung function and repair long after the virus itself has disappeared.” Somehow the virus had acquired the capacity to upregulate expression of CYP19A1.
Only two COVID-19 positive females showed increased expression of this gene. The menopause status of these women, or whether they were on hormone replacement therapy was not known. That could be important because female hormones have a protective effect for cardiovascular disease, which women often lose after going through menopause, especially if they don’t start hormone replacement therapy. That sex-specific protection might also extend to COVID-19 and merits further study.
The team was able to confirm their findings in golden hamsters, the animal model of choice for studying COVID-19. Testosterone levels in male animals dropped 5-fold three days after infection and began to recover as viral levels declined. CYP19A1 transcription increased up to 15-fold in the lungs of the male but not the females. The study authors wrote, “Virus replication in the male lungs was negatively associated with testosterone levels.”
The medical community studying COVID-19 has slowly come to recognize the importance of adipose tissue, or fat cells. They are known to express abundant levels of CYP19A1 and play a significant role as metabolic tissue in COVID-19. Gabriel adds, “One of the key findings of our study is that upon SARS-CoV-2 infection, the lung suddenly turns into a metabolic organ by highly expressing” CYP19A1.
She also found evidence that SARS-CoV-2 can infect the gonads of hamsters, thereby likely depressing circulating levels of sex hormones. The researchers did not have autopsy samples to confirm this in humans, but others have shown that the virus can replicate in those tissues.
A possible treatment
Back in the lab, substituting low and high doses of testosterone in SARS-COV-2 infected male hamsters had opposite effects depending on testosterone dosage used. Gabriel says that hormone levels can vary so much, depending on health status and age and even may change throughout the day, that “it probably is much better to inhibit the enzyme” produced by CYP19A1 than try to balance the hormones.
Results were better with letrozole, a drug approved to treat hypogonadism in males, which reduces estradiol levels. The drug also showed benefit in male hamsters in terms of less severe disease and faster recovery. She says more details need to be worked out in using letrozole to treat COVID-19, but they are talking with hospitals about clinical trials of the drug.
Gabriel has proposed a four hit explanation of how COVID-19 can be so deadly for men: the metabolic quartet. First is the genetic risk factor of CYP19A1 (Thr201Met), then comes SARS-CoV-2 infection that induces even greater expression of this gene and the deleterious increase of estradiol in the lung. Age-related hypogonadism and the heightened inflammation of obesity, known to affect CYP19A1 activity, are contributing factors in this deadly perfect storm of events.
Studying host genetics, says Gabriel, can reveal new mechanisms that yield promising avenues for further study. It’s also uniting different fields of science into a new, collaborative approach they’re calling “infection endocrinology,” she says.